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_MS2 Cardio > 8/5- Arrhythmias > Flashcards

8/5- Arrhythmias Flashcards

1
Q

What is a normal QRS complex time/width? Long?

A

Normal is ~120 ms, long is anything over about 140

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2
Q

What are the 3 steps in diagnosing any arrhythmia?

A
  1. Determine if the QRS complexes are narrow or wide
  2. Determine if the QRS complexes or regular or irregular (distance of more than 1/2 a box between complexes)
  3. Determine if P waves or evidence of atrial activity are present (relation between P wave and QRS)
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3
Q

What are possible arrhythmias if QRS complexes are narrow and regular?

A
  • Sinus tachycardia
  • Atrial tachycardia
  • Atrial flutter
  • AVNRT
  • AVRT
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4
Q

What are possible arrhythmias if QRS complexes are narrow and irregular?

A
  • MAT
  • Atrial flutter with variable conduction
  • Atrial fibrillation
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5
Q

What are possible arrythmias if QRS complexes are wide?

A
  • SVT with BBB
  • Ventricular tachycardia
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6
Q

What is this? Analyze

A
  • HR ~ 150 bpm (tachycardia)
  • Positive upright (normal) P waves in front of every QRS complex (1:1 P:QRS ratio)
  • QRS is nice and slim; no conduction problem down from the atrium
  • Limited analysis because there’s only 1 lead, but this P wave morphology may indicated sinus wave tachycardia

Most likely: sinus tachycardia

  • This is just a rate problem
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7
Q

What is sinus tachycardia typically a response to?

A

Sinus tachycardia is almost always a physiologic response

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8
Q

What may cause sinus tachycardia?

A
  • Hypotension
  • Hypovolemia/anemia/acute bleed
  • MI/depressed EF/tamponade
  • Hypoxemia
  • Fever
  • Anxiety/pain
  • Medications
  • (Hyperthyroidism)
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9
Q

What other types of sinus tachycardia are present (rarely)?

A
  • Sinus node reentrant tachycardia
  • Non paroxysmal sinus tachycardia
  • Postural orthostatic tachycardia syndrome (POTS)
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10
Q

What is this?

A
  • P wave present before every QRS complex (this is probably ~ lead II: P waves are negative)
  • P wave looks a little uncharacteristic (although only 1 lead here): ectopic P waves (anything originating from any other place than the sinus node)

Ectopic atrial tachycardia

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11
Q

What are some common causes of atrial tachycardia?

A
  • Structural (atrial) heart disease/diseased atria
  • Sympathetic stimulation
  • Toxins/drugs
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12
Q

What is the heart rate range for atrial tachycardia?

A

120-250 bpm (typically ~ 160)

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13
Q

T/F: Atrial tachycardia typically causes hemodynamic compromise?

A

False; atrial tachycardia usually does NOT cause hemodynamic compromise

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14
Q

Treatments for atrial tachycardia?

A
  • Withdraw sympathetic stimuli/drugs
  • Rarely (if ever) use antiarrhythmics
  • Often does not respond to cardioversion
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15
Q

What is this? Analyze

A

Atrial Tachycardia with Block (PAT with Block)

  • Arrows pointing at P waves (negative here)
  • No 1:1 conduction here; P waves too fast and ventricles can’t respond to each one. You basically see conduction every 4th P wave
  • “Block” from inability of AV node to handle atrial tachycardia rate; may be protective, but bad if it causes heart rate to drop too low
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16
Q

What could cause atrial tachycardia with block (PAT with block)?

A

Digoxin toxicity

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17
Q

What is a common treatment for really any type of tachycardia?

A

Catheter ablation

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18
Q

What is this? Analyze

A
  • Continuous undulation of isoelectric line; no straightish segment between P waves
  • Sawtooth line pattern of isoelectric line

Atrial flutter

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19
Q

What does the conduction pattern look like in atrial flutter?

A

Depolarization is traveling continuously in an atrial circuit; there’s basically no free atrial activation that would create straight isoelectric line between P waves

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20
Q

What may cause atrial flutter?

A

Diseased or dilated atria

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21
Q

What is the heart rate in atrial flutter?

A

Usually 300 (with 2:1 AV block)

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22
Q

Treatment for atrial flutter?

A
  • Unstable: synchronized cardioversion (shock the pt)
  • Slow AV conduction (Metoprolol, Verapamil or diltiazem, not digoxin acutely)
  • Convert back to sinus
  • Recently, anticoagulate like AF (stagnant blood in parts of the atria may cause clots… -> brain)
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23
Q

What is this? Analyze

A
  • Narrow complex tachycardia; regular
  • Don’t see clear P wave

Narrow complex QRS tachycardia with no regular P wave; there are 2 possibilities from here:

  • AVNRT or AVRT??
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24
Q

What is AVNRT (name)? What is the conduction pathway?

A

AV Nodal Re-Entrant Tachycardia (AVNRT)

  • Rhythm originates in AV node
  • Atria and ventricles are activated almost simultaneously, thus P and QRS occur almost the same time (P waves can’t be observed)
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25
Q

What causes AVNRT?

A

“Micro-reentrant pathway”

  • Usually “paroxysmal”, often triggered by PAC
  • Rarely correlated with any heart disease; occurs in structurally normal hearts (?)
26
Q

Treatment for AVNRT?

A

- Unstable: cardiovert

- Block AV conduction:

—Vagal-enhancing maneuvers

—Adenosine (6 mg,12,12): almost always works

—Verapamil or Diltiazem

—Beta blockers

- Ablation

27
Q

What is this? Analyze

A
  • Cousin to AVNRT, but this AVRT
  • There is a P wave (outside the QRS; commonly not seen)
28
Q

What is AVRT? What is the conduction pathway?

A

AV Re-entrant Tachycardia (AVRT)

  • Both atria and ventricle are equal participants in tachycardia
  • Conduction happens in reverse from ventricle to atrium; don’c contract simultaneously (ventricles first)
  • May see retrograde P wave distorting ST segment
  • This is orthodromic (anti-dromic could have reversed conduction path and weird ventricle pattern)
29
Q

What causes AVRT?

A

“macro reentrant loop” involving bypass tract

  • Usually “paroxysmal”
30
Q

Orthodromic conduction (shown earlier) occurs in ___% of cases while antidromic (may resemble VT) occurs in ___%

A

Orthodromic: 90-95%

Antidromic: 5%

31
Q

Treatment for AVRT?

A
  • Unstable: cardiovert
  • Stable: block or slow AV node conduction
  • Ultimately: ablation
32
Q

The following distinguishing characteristics of narrow complex regular tachycardia point to what types of arrhythmias?

  • Normal P waves ->
  • Abnormal P waves ->
  • Flutter waves ->
  • No atrial activity ->
A
  • Normal P waves -> sinus tachycardia
  • Abnormal P waves -> atrial tachycardia
  • Flutter waves -> atrial flutter
  • No atrial activity -> AVNRT or AVRT
33
Q

What is this?

A

Multifocal Atrial Tachycardia (MAT)

34
Q

Conduction pattern in MAT?

A
35
Q

How can MAT be diagnosed?

A
  • 3 or more distinct P waves
  • Ventricular rate 100
36
Q

What cuases MAT?

A

Usually occurs in pts with pulmonary disease, esp COPD

37
Q

Treatment for MAT?

A
  • TREAT UNDERLYING DISEASE
  • Try to decrease sympathomimetics
  • Attempts to suppress arrhythmia or block AV conduction are usually futile*
38
Q

What is this?

A

Atrial flutter (with variable conduction)

39
Q

What is the conduction pattern in atrial flutter?

A
40
Q

What is this?

A

Atrial fibrillation

41
Q

What is the conduction pattern in atrial fibrillation?

A
  • May also be due to focus in pulmonary vein
42
Q

What may cause atrial fibrillation?

A
  • HTN
  • Ischemia/CAD
  • Atrial dilation (MV disease, etc)
  • Toxins
  • Pericarditis
  • Pulmonary emoblus
  • Hyperthyroidism
  • Vagal or sympathetic mediated
  • (Pulmonary vein)

Many AF causes may be caused by focus in pulmonary vein

43
Q

Nomenclature in atrial fibrillation:

  • Paroxysmal, episodic:
  • Persistent:
  • Permanent:
A

Nomenclature in atrial fibrillation:

- Paroxysmal, episodic: AF converts to NSR spontaneously

- Persistent: AF terminates only after intervention

- Permanent: AF resists attempts to restore NST

44
Q

Treatment for atrial fibrillation?

A
  • Unstable: cardiovert
  • Stable: slow ventricular response rate or electively cardiovert
  • If in afib > 48 hrs or unknown time, anticoagulate or obtain TEE to r/o thrombus; then cardioversion and/or ibutilide
45
Q

Recap: The following distinguishing characteristics of narrow irregular tachycardia point to what types of arrhythmias?

  • Multiple different P waves ->
  • Flutter waves ->
  • No atrial activity ->
A

Narrow irregular tachycardias:

  • Multiple different P waves -> MAT
  • Flutter waves -> atrial flutter
  • No atrial activity -> atrial fibrillation
46
Q

What is this? Analyze

A

“Boringly regular” QRS complexes in WCTs due to SVT

47
Q

What is this? Analyze

A

Slightly irregular QRS complexes in VT

48
Q

What is the conduction pattern in atrial and ventricular dissociation in ventricular tachycardia?

(P wave dissociation/AV dissociation)

A
49
Q

What is this? Analyze

A

VT with AV dissociation

50
Q

What is the conduction pattern in ventricular tachycardia?

A
51
Q

What may cause ventricular tachycardia?

A
  • Acute ischemia or acute myocardial infarction
  • Reentry around old scar or aneurysm
  • Medications that prolong QT interval
52
Q

Treatment for ventricular tachycardia?

A
  • Unresponsive or pulseless: defibrillation
  • Unstable: synchronized cardioversion
  • Stable: antiarrhtyhmic agents
53
Q

What is this?

A

Ventricular tachycardia: Torsades de Pointes

54
Q

What is this?

A

Atrial tachycardia with block; flutter

55
Q

What is this?

A

Multifocal atrial tachycardia

  • see 3 or more morphologies
56
Q

What is this?

A

Sinus tachycardia with bundle branch block

  • Rate here is little more than 100
  • Note aVL and V1 leads
57
Q

What is this?

A

?

58
Q

What is this?

A

?

59
Q

What is this?

A

?

60
Q

What is this?

A

?

61
Q

Side effects of antiarrhythmic therapy?

A
  • Negative inotropy
  • QT prolongation and torsades de pointes
  • Pro-arrhythmic

* Suppressing PVCs increases death

* Treating atrial fibrillation by trying to suppress the arrhythmia is not better than anticoagulating and controlling the rate

* AICDs (defibrillators) are better than antiarrhyhmics in pts with ventricular tachycardia (VT)

62
Q

What is Amiodarone?

A

Drug for antiarrhythmic therapy

  • Beta blocking, Ca-channel blocking, and direct; acts on SA node, AV node, atrial and ventricular tissues
  • When starting: follow for bradycardia and heart block
  • Longer term (q6 mo): liver function tests, thyroid function tests (esp TSH), CXR (pulmonary fibrosis)
  • Important drug interactions: increases INR, increases digoxin level
  • Useful loading dose: bolus, then 1 mg/kg/hr; 400 BID-TID
  • Usual maintenance dosing:

—Atrial arrhythmias; 100-200 qD

—Ventricular arrhythmias: 200-400 qD

_MS2 Cardio (35 decks)

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